http://www.johnsonupdaydowndaydiet.samsbiz.com/content/00/01/53/97/83/userimages/ADCR%20article.pdf

Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma.

Background Psychologic stress modifies immune function and cytokine production. Objective We examined relationships between caregiver stress on the following markers of early childhood immune response: (1) IgE expression (n = 215); (2) mitogen-induced and allergen-specific ( Dermatophagoides farinae [Der f 1] and cockroach [Bla g 2]) proliferative response (n = 114); and (3) subsequent cytokine expression (INF-γ, TNF-α, IL-10, and IL-13) in a prospective birth cohort predisposed to atopy. Methods Caregiver stress was measured at 2-month intervals for the first 2 years of life and yearly thereafter by using the Perceived Stress Scale. A subsequent blood sample obtained from the children (median age, 2.1 years; range, 18-32 months) was analyzed for total serum IgE level and allergen-induced proliferation quantified as the stimulation index (SI; mean thymidine incorporation of the stimulated sample divided by that of the unstimulated sample). The relationship between stress and the proliferative response (SI >3 vs SI ≤3), and total IgE level (≤100 IU/mL vs >100 IU/mL) was examined by using logistic regression. The relationship between cytokine levels and stress was analyzed by using linear regression. Results In adjusted analyses higher caregiver stress in the first 6 months after birth was associated with a Der f 1 SI of greater than 3 (odds ratio [OR], 1.5; 95% CI, 1.0-2.3) and nominally associated with a Bla g 2 SI of greater than 3 (OR, 1.13; 95% CI, 0.7-1.8). Higher stress between ages 6 and 18 months was associated with a high total IgE level (OR, 2.03; 95% CI, 1.1-3.6). Higher stress was significantly associated with increased production of TNF-α, with a suggested trend between higher stress and reduced INF-γ production. Conclusion Increased stress in early childhood was associated with an atopic immune profile in these children predisposed to atopy-asthma.

https://www.jacionline.org/article/S0091-6749(04)01164-9/pdf

Chronic caregiver stress and IgE expression, allergen-induced proliferation, and cytokine profiles in a birth cohort predisposed to atopy

Asthma has been associated with increased cardiovascular disease (CVD) risk. The authors ascertained the association of asthma with CVD and the roles that sex, concurrent allergy, and asthma medications may play in this association. They assembled a cohort of 203,595 Northern California adults with asthma and a parallel asthma-free referent cohort (matched 1:1 on age, sex, and race/ethnicity); both cohorts were followed for incident nonfatal or fatal CVD and all-cause mortality from January 1, 1996, through December 31, 2008. Each cohort was 66% female and 47% white. After adjustment for age, sex, race/ethnicity, cardiac risk factors, and comorbid allergy, asthma was associated with a 1.40-fold (95% confidence interval (CI): 1.35, 1.45) increased hazard of coronary heart disease, a 1.20-fold (95% CI: 1.15, 1.25) hazard of cerebrovascular disease, a 2.14-fold (95% CI: 2.06, 2.22) hazard of heart failure, and a 3.28-fold (95% CI: 3.15, 3.41) hazard of all-cause mortality. Stronger associations were noted among women. Comorbid allergy predicted CVD but did not synergistically increase the CVD risk associated with asthma. Only asthma patients using asthma medications (particularly those on oral corticosteroids alone or in combination) were at enhanced risk of CVD. In conclusion, asthma was prospectively associated with increased risk of major CVD. Modifying effects were noted for sex and asthma medication use but not for comorbid allergy.

Adult Asthma and Risk of Coronary Heart Disease, Cerebrovascular Disease, and Heart Failure: A Prospective Study of 2 Matched Cohorts

Background EXCELS, a postmarketing observational cohort study, was a commitment to the US Food and Drug Administration to assess the long-term safety of omalizumab in an observational setting, focusing predominantly on malignancies. Objective The aim of this study was to examine a potential association between omalizumab and cardiovascular (CV)/cerebrovascular (CBV) events in EXCELS. Methods Patients (≥12 years of age) with moderate to severe allergic asthma and who were being treated with omalizumab (n = 5007) or not (n = 2829) at baseline were followed up for ≤5 years. Analyses included overall CV/CBV events, but focused on the subset of arterial thromboembolic events (ATEs), comprising CV death, myocardial infarction, ischemic stroke, transient ischemic attack, and unstable angina. A prespecified analysis of the end point of ATE was conducted to control for available potential confounders. A blinded independent expert panel adjudicated all events. Results At baseline, the 2 cohorts had similar demographic characteristics, but severe asthma was more common in the omalizumab versus the non-omalizumab group (50% vs 23%). Omalizumab-treated patients had a higher rate of CV/CBV serious adverse events (13.4 per 1,000 person years [PYs]) than did non–omalizumab-treated patients (8.1 per 1,000 PYs). The ATE rates per 1,000 PYs were 6.66 (101 patients/15,160 PYs) in the omalizumab cohort and 4.64 (46 patients/9,904 PYs) in the non-omalizumab cohort. After control for available confounding factors, the hazard ratio was 1.32 (95% CI, 0.91-1.91). Conclusion This observational study demonstrated a higher incidence rate of CV/CBV events in the omalizumab versus the non-omalizumab cohort. Differences in asthma severity between cohorts likely contributed to this imbalance, but some increase in risk cannot be excluded.

Cardiovascular and cerebrovascular events among patients receiving omalizumab: Results from EXCELS, a prospective cohort study in moderate to severe asthma

Background TNF is thought to contribute to airway hyperreactivity (AHR) and airway inflammation in asthma. However, studies with TNF-deficient or TNF receptor–deficient mice have not produced a clear picture of the role of TNF in the AHR associated with allergic inflammation in the mouse. Objective We used a genetic approach to investigate the contributions of TNF to antigen-induced AHR and airway inflammation in mice on the C57BL/6 background. Methods We analyzed features of airway allergic inflammation, including antigen-induced AHR, in C57BL/6 wild-type and TNF −/− mice, using 2 different methods for sensitizing the mice to ovalbumin (OVA). Results In mice sensitized to OVA administered with the adjuvant aluminum hydroxide (alum), which develop IgE-independent and mast cell–independent allergic inflammation and AHR, we found no significant differences in OVA-induced AHR in C57BL/6-TNF −/− versus wild-type mice. By contrast, in mice sensitized to OVA without alum, which develop allergic inflammation that is significantly mast cell–dependent, C57BL/6-TNF −/− mice exhibited significant reductions versus wild-type mice in OVA-induced AHR to methacholine; numbers of lymphocytes, neutrophils, and eosinophils in bronchoalveolar lavage fluid; levels of myeloperoxidase, eosinophil peroxidase, and the cytokines IL-4, IL-5, and IL-17 in lung tissue; and histologic evidence of pulmonary inflammation. Conclusion In pulmonary allergic inflammation induced in mice immunized with OVA without alum, TNF significantly contributes to several features of the response, including antigen-induced inflammation and AHR. Clinical implications Our findings in mice support the hypothesis that TNF can promote the allergic inflammation and AHR associated with asthma.

TNF can contribute to multiple features of ovalbumin-induced allergic inflammation of the airways in mice.

The aim of the study was to investigate the activation of inflammatory mediators interleukin (IL)-4, IL-5, and IL-8; immunoglobulin E (IgE); and eosinophil cationic protein (ECP) and to evaluate the regulatory role of the tumor necrosis system (TNF) system in bronchial hyperreactivity. Adults who had suffered from bronchial asthma in childhood but who had been symptom free for at least 3 years were examined together with their children who did not have asthma. The serum concentrations of TNF-alpha, soluble TNF receptor 1 (sTNF-R1), TNF-R2, IL-4, IL-5, IL-8, ECP, and IgE were studied in symptom-free adults (n = 22) and their children (n = 22) with bronchial hyperreactivity. Nonhyperreactive individuals with a similar medical history (adults, n = 17; children, n = 20) served as controls. Significantly elevated serum TNF-alpha (X +/- SD: 5.13 +/- 1.37 pg/mL versus 3.91 +/- 0.61 pg/mL; p < 0.0001), sTNF-R1 (X +/- SD: 1.37 +/- 0.28 ng/mL versus 1.16 +/- 0.13 ng/mL; p = 0.0002), and sTNF-R2 (X +/- SD: 0.78 +/- 0.42 ng/mL versus 0.43 +/- 0.41 ng/mL; p = 0.0001); IL-4 (X +/- SD: 4.05 +/- 1.02 pg/mL versus 3.34 +/- 0.84 pg/mL; p = 0.0016); IgE (X +/- SD: 390.1 +/- 361.4 KU/L versus 130.2 +/- 166.1 KU/L; p = 0.0001); and ECP (X +/- SD: 17.57 +/- 11.03 micrograms/L versus 10.65 +/- 6.01 micrograms/L; p = 0.0016) concentrations were measured in the subjects with bronchial hyperreactivity as compared with the nonhyperreactive group. Significant positive linear correlations were observed for the bronchial hyperreactive group between the concentrations of TNF-alpha and ECP, TNF-alpha and sTNF-R1, TNF-alpha and IL-8, sTNF-R1 and ECP, sTNF-R1 and IL-8, and sTNF-R2 and IL-8. Moreover, the TNF-alpha and sTNF-R2 levels correlated with the airway reactivity in the hyperreactive group. We suggest that the elevated cytokine levels indicate activation of the immune system in individuals who were previously asthmatic, but recovered, and are now symptom free and in their children with nonasthmatic bronchial hyperreactivity. The TNF system may play a key role in the pathomechanism of bronchial hyperreactivity.

Relationship between the tumor necrosis factor system and the serum interleukin-4, interleukin-5, interleukin-8, eosinophil cationic protein, and immunoglobulin E levels in the bronchial hyperreactivity of adults and their children

Role of TNF-α and its 55 and 75 kDa receptors in bronchial hyperreactivity

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

A. Halász

Author Tools

Chat about Author

Papers

Relationship between the tumor necrosis factor system and the serum interleukin-4, interleukin-5, interleukin-8, eosinophil cationic protein, and immunoglobulin E levels in the bronchial hyperreactivity of adults and their children

Role of TNF-α and its 55 and 75 kDa receptors in bronchial hyperreactivity